Cardioplegia Principles And Problems

Konventionelle und molekularpathologische Untersuchungen während und nach klinischer Herztransplantation

“…B. als Kontraktionsb~mder in zentralen Probenanteilen (vgl. Die in dieser Arbeit atffgezeigten Ergebnisse basieren auf umfangreichen experimentellen Vorarbeiten, bet denen ultrastrukturetle Befunde mit funktionellen und metabolischen Daten verglichen wurden (5,6,14,24,37,46). 6A), in denen Schnittkantenlfisionen sicher auszuschliel3en sind (45).…”

“…6A), in denen Schnittkantenlfisionen sicher auszuschliel3en sind (45). Konservierungs-Verfahren besonders geeignet sind (5,6,14,36,46). Jedoch dienen die w~ihrend HTx erhobenen quantitativen Daten als Ausgangsweft ffir Vefiinderungen im postoperativen Verlauf (27,32,41,42).…”

Intracellular sodium activity and Bretschneider's cardioplegia: Continuous measurement by ionselective microelectrodes at initial equilibration

“…The cardioplegic solution "HTK" proposed by Bretschneider and co-workers fulfills these requirements (4,6,22). Reduction of extracellular sodium to 15 mM leads to cardiac arrest by depriving substrate for the fast sodium upstroke of the action potential, supported by a *) Supported by the DFG, SFB 330 "Organprotektion".…”

“…For reasons of ionic balance, the sodium reduction demands a further lowering of Ca in the perfusate, since otherwise a massive Ca overload and unfavorable stimulation of cellular metabolism would occur. Furthermore, the Bretschneider principle of a sodium-poor, nominally calcium-free (15-20 ixmolfl) cardioplegic solution requires osmotic adjustment, which is accomplished by the addition of histidine/histidine-HC1, a buffering system having an appropriate pk for the pH desired and giving a large extracellular buffer capacity (22). This enhanced buffer capacity slows tissue acidification throughout the ischemic period due to the production of lactic acid (19,34), thereby delaying self inhibition of anaerobic glycolysis (22).…”

“…Furthermore, the Bretschneider principle of a sodium-poor, nominally calcium-free (15-20 ixmolfl) cardioplegic solution requires osmotic adjustment, which is accomplished by the addition of histidine/histidine-HC1, a buffering system having an appropriate pk for the pH desired and giving a large extracellular buffer capacity (22). This enhanced buffer capacity slows tissue acidification throughout the ischemic period due to the production of lactic acid (19,34), thereby delaying self inhibition of anaerobic glycolysis (22). These extreme changes of extracellular ionic composition can be expected to cause alterations of intracellular pH and sodium activity, which have been found after simply reducing extracellular Na in Tyrode's solution (16).…”